Pub Date : 2023-10-01Epub Date: 2023-09-06DOI: 10.4078/jrd.2023.0041
Se Hee Kim, Sang-Hoon Lee
Ankylosing spondylitis (AS) is an autoinflammatory disease that manifests with the unique feature of enthesitis. Gut microbiota, HLA-B*27, and biomechanical stress mutually influence and interact resulting in setting off a flame of inflammation. In the HLA-B*27 positive group, dysbiosis in the gut environment disrupts the barrier to exogenous bacteria or viruses. Additionally, biomechanical stress induces inflammation through enthesial resident or gut-origin immune cells. On this basis, innate and adaptive immunity can propagate inflammation and lead to chronic disease. Finally, bone homeostasis is regulated by cytokines, by which the inflamed region is substituted into new bone. Agents that block cytokines are constantly being developed to provide diverse therapeutic options for preventing the progression of inflammation. In addition, some antibodies have been shown to distinguish disease selectively, which support the involvement of autoimmune immunity in AS. In this review, we critically analyze the complexity and uniqueness of the pathogenesis with updates on the findings of immunity and provide new information about biologics and biomarkers.
{"title":"Updates on ankylosing spondylitis: pathogenesis and therapeutic agents.","authors":"Se Hee Kim, Sang-Hoon Lee","doi":"10.4078/jrd.2023.0041","DOIUrl":"https://doi.org/10.4078/jrd.2023.0041","url":null,"abstract":"<p><p>Ankylosing spondylitis (AS) is an autoinflammatory disease that manifests with the unique feature of enthesitis. Gut microbiota, HLA-B*27, and biomechanical stress mutually influence and interact resulting in setting off a flame of inflammation. In the HLA-B*27 positive group, dysbiosis in the gut environment disrupts the barrier to exogenous bacteria or viruses. Additionally, biomechanical stress induces inflammation through enthesial resident or gut-origin immune cells. On this basis, innate and adaptive immunity can propagate inflammation and lead to chronic disease. Finally, bone homeostasis is regulated by cytokines, by which the inflamed region is substituted into new bone. Agents that block cytokines are constantly being developed to provide diverse therapeutic options for preventing the progression of inflammation. In addition, some antibodies have been shown to distinguish disease selectively, which support the involvement of autoimmune immunity in AS. In this review, we critically analyze the complexity and uniqueness of the pathogenesis with updates on the findings of immunity and provide new information about biologics and biomarkers.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3a/9f/jrd-30-4-220.PMC10509639.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41141435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-01Epub Date: 2023-08-09DOI: 10.4078/jrd.2023.0030
Jung Hee Koh, Bong-Woo Lee, Wan-Uk Kim
Objective: To assess the effects of biological and targeted synthetic disease-modifying antirheumatic drugs (DMARDs) on lipid profiles in patients with moderate-to-severe rheumatoid arthritis (RA).
Methods: This retrospective single-center observational study included patients with RA taking a tumor necrosis factor-α inhibitor (TNFi), abatacept, tocilizumab, or a Janus kinase inhibitor (JAKi) for at least 6 months. Changes in lipid profile were assessed at 6 months after the start of treatment, and associations between changes in lipid profiles and clinical efficacy, concomitant medications, and comorbidities were evaluated.
Results: This study included 114 patients treated with TNFi, 81 with abatacept, 103 with tocilizumab, and 89 with JAKi. The mean percentage change (from baseline to 6 months) in total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and non-HDL-C levels was higher in those taking tocilizumab and JAKi than in those taking TNFi and abatacept. A significant change in non-HDL-C was associated with JAKi (versus TNFi odds ratio [OR], 3.228; 95% confidence interval [CI], 1.536~6.785), tocilizumab (versus TNFi OR, 2.203; 95% CI, 1.035~4.689), and statins (OR, 0.487; 95% CI, 0.231~1.024). However, changes in disease activity in 28 joints were not associated with a significant change in non-HDL-C.
Conclusion: Tocilizumab- and JAKi-associated increases in serum non-HDL-C levels were observed regardless of changes in disease activity. Statins are recommended for RA patients showing a significant increase in cholesterol levels after initiating biological and targeted synthetic DMARDs.
{"title":"Changes in the cholesterol profile of patients with rheumatoid arthritis treated with biologics or Janus kinase inhibitors.","authors":"Jung Hee Koh, Bong-Woo Lee, Wan-Uk Kim","doi":"10.4078/jrd.2023.0030","DOIUrl":"https://doi.org/10.4078/jrd.2023.0030","url":null,"abstract":"<p><strong>Objective: </strong>To assess the effects of biological and targeted synthetic disease-modifying antirheumatic drugs (DMARDs) on lipid profiles in patients with moderate-to-severe rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>This retrospective single-center observational study included patients with RA taking a tumor necrosis factor-α inhibitor (TNFi), abatacept, tocilizumab, or a Janus kinase inhibitor (JAKi) for at least 6 months. Changes in lipid profile were assessed at 6 months after the start of treatment, and associations between changes in lipid profiles and clinical efficacy, concomitant medications, and comorbidities were evaluated.</p><p><strong>Results: </strong>This study included 114 patients treated with TNFi, 81 with abatacept, 103 with tocilizumab, and 89 with JAKi. The mean percentage change (from baseline to 6 months) in total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and non-HDL-C levels was higher in those taking tocilizumab and JAKi than in those taking TNFi and abatacept. A significant change in non-HDL-C was associated with JAKi (versus TNFi odds ratio [OR], 3.228; 95% confidence interval [CI], 1.536~6.785), tocilizumab (versus TNFi OR, 2.203; 95% CI, 1.035~4.689), and statins (OR, 0.487; 95% CI, 0.231~1.024). However, changes in disease activity in 28 joints were not associated with a significant change in non-HDL-C.</p><p><strong>Conclusion: </strong>Tocilizumab- and JAKi-associated increases in serum non-HDL-C levels were observed regardless of changes in disease activity. Statins are recommended for RA patients showing a significant increase in cholesterol levels after initiating biological and targeted synthetic DMARDs.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3c/07/jrd-30-4-234.PMC10509638.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41162557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-01Epub Date: 2023-08-30DOI: 10.4078/jrd.2023.0020
Sang Wan Chung, Joo Ho Lee, You-Jung Ha, Eun Ha Kang, Yun Jong Lee
Behçet syndrome (BS) is a chronic inflammatory disease with multiorgan manifestations. However, muscular involvement in BS has rarely been reported. Herein, we report the case of a 30-year-old male with BS who had recurring pain and swelling of the lower legs. The patient was administered antibiotics on several occasions as the condition was misinterpreted to be infectious myositis. Magnetic resonance imaging revealed myofascial involvement with focal necrotic lesions, and muscle biopsy revealed acute suppurative myositis with perivascular infiltration of polymorphonuclear leukocytes. His symptoms improved after treatment with corticosteroids. Azathioprine and colchicine therapy was beneficial for preventing further relapse after short-term corticosteroid treatment. Therefore, BS should be considered in the differential diagnosis of focal suppurative myofasciitis.
{"title":"Recurrent focal myofasciitis of Behçet syndrome mimics infectious myofasciitis: a case report.","authors":"Sang Wan Chung, Joo Ho Lee, You-Jung Ha, Eun Ha Kang, Yun Jong Lee","doi":"10.4078/jrd.2023.0020","DOIUrl":"https://doi.org/10.4078/jrd.2023.0020","url":null,"abstract":"<p><p>Behçet syndrome (BS) is a chronic inflammatory disease with multiorgan manifestations. However, muscular involvement in BS has rarely been reported. Herein, we report the case of a 30-year-old male with BS who had recurring pain and swelling of the lower legs. The patient was administered antibiotics on several occasions as the condition was misinterpreted to be infectious myositis. Magnetic resonance imaging revealed myofascial involvement with focal necrotic lesions, and muscle biopsy revealed acute suppurative myositis with perivascular infiltration of polymorphonuclear leukocytes. His symptoms improved after treatment with corticosteroids. Azathioprine and colchicine therapy was beneficial for preventing further relapse after short-term corticosteroid treatment. Therefore, BS should be considered in the differential diagnosis of focal suppurative myofasciitis.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a5/8f/jrd-30-4-268.PMC10509642.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41174711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jennifer Jooha Lee, Ji Soo Lee, Min Kyung Chung, Joong Kyong Ahn, Hyo-Jin Choi, Seung-Jae Hong, Chong-Hyeon Yoon, Su-Hyun Kim, Kyung-Hwan Jeong, Jong-Woo Kim, Bo-Yeon Kim, Jin-Ho Shin, Woo Gyu Kim, Soo-Young Kim, Hyun-Jung Kim, Jeong-Soo Song, Jae-Bum Jun, Hyun-Ah Park, Shung Chull Chae, Bum Soon Choi, Tae Nyun Kim, Hyun Ah Kim
Gout is the most common form of arthritis, with the prevalence increasing worldwide. The present treatment guidelines provide recommendations for the appropriate treatment of acute gout, management during the inter-critical period, and prevention of chronic complications. The guidelines were developed based on evidence-based medicine and draft recommendations finalized after expert consensus. These guidelines are designed to provide clinicians with clinical evidence to enable efficient treatment of gout.
{"title":"Korean guidelines for the management of gout.","authors":"Jennifer Jooha Lee, Ji Soo Lee, Min Kyung Chung, Joong Kyong Ahn, Hyo-Jin Choi, Seung-Jae Hong, Chong-Hyeon Yoon, Su-Hyun Kim, Kyung-Hwan Jeong, Jong-Woo Kim, Bo-Yeon Kim, Jin-Ho Shin, Woo Gyu Kim, Soo-Young Kim, Hyun-Jung Kim, Jeong-Soo Song, Jae-Bum Jun, Hyun-Ah Park, Shung Chull Chae, Bum Soon Choi, Tae Nyun Kim, Hyun Ah Kim","doi":"10.4078/jrd.2023.0029","DOIUrl":"10.4078/jrd.2023.0029","url":null,"abstract":"<p><p>Gout is the most common form of arthritis, with the prevalence increasing worldwide. The present treatment guidelines provide recommendations for the appropriate treatment of acute gout, management during the inter-critical period, and prevention of chronic complications. The guidelines were developed based on evidence-based medicine and draft recommendations finalized after expert consensus. These guidelines are designed to provide clinicians with clinical evidence to enable efficient treatment of gout.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ae/0c/jrd-30-3-141.PMC10351368.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9851656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyun Jung Kim, Byeongzu Ghang, Jinseok Kim, Hyeong Sik Ahn
Objective: The extent of regional variations in cardiovascular risk and associated risk factors in patients with gout in South Korea remains unclear. Therefore, we aimed to investigate the risk of major cardiovascular events in gout patients in different regions.
Methods: This was a nationwide cohort study based on the claims database of the Korean National Health Insurance and the National Health Screening Program. Patients aged 20 to 90 years newly diagnosed with gout after January 2012 were included. After cardiovascular risk profiles before gout diagnosis were adjusted, the relative risks of incident cardiovascular events (myocardial infarction, cerebral infarction, and cerebral hemorrhage) in gout patients in different regions were assessed.
Results: In total, 231,668 patients with gout were studied. Regional differences in cardiovascular risk profiles before the diagnosis were observed. Multivariable analysis showed that patients with gout in Jeolla/Gwangju had a significantly high risk of myocardial infarction (adjusted hazard ratio [aHR], 1.27; 95% confidence interval [CI], 1.02~1.56; p=0.03). In addition, patients with gout in Gangwon (aHR, 1.38; 95% CI, 1.09~1.74; p<0.01), Jeolla/Gwangju (aHR, 1.41; 95% CI, 1.19~1.67; p<0.01), and Gyeongsang/Busan/Daegu/Ulsan (aHR, 1.37; 95% CI, 1.19~1.59; p<0.01) had a significantly high risk of cerebral infarction.
Conclusion: We found there were regional differences in cardiovascular risk and associated risk factors in gout patients. Physicians should screen gout patients for cardiovascular risk profiles in order to facilitate prompt diagnosis and treatment.
{"title":"Regional variations of cardiovascular risk in gout patients: a nationwide cohort study in Korea.","authors":"Hyun Jung Kim, Byeongzu Ghang, Jinseok Kim, Hyeong Sik Ahn","doi":"10.4078/jrd.2023.0011","DOIUrl":"https://doi.org/10.4078/jrd.2023.0011","url":null,"abstract":"<p><strong>Objective: </strong>The extent of regional variations in cardiovascular risk and associated risk factors in patients with gout in South Korea remains unclear. Therefore, we aimed to investigate the risk of major cardiovascular events in gout patients in different regions.</p><p><strong>Methods: </strong>This was a nationwide cohort study based on the claims database of the Korean National Health Insurance and the National Health Screening Program. Patients aged 20 to 90 years newly diagnosed with gout after January 2012 were included. After cardiovascular risk profiles before gout diagnosis were adjusted, the relative risks of incident cardiovascular events (myocardial infarction, cerebral infarction, and cerebral hemorrhage) in gout patients in different regions were assessed.</p><p><strong>Results: </strong>In total, 231,668 patients with gout were studied. Regional differences in cardiovascular risk profiles before the diagnosis were observed. Multivariable analysis showed that patients with gout in Jeolla/Gwangju had a significantly high risk of myocardial infarction (adjusted hazard ratio [aHR], 1.27; 95% confidence interval [CI], 1.02~1.56; p=0.03). In addition, patients with gout in Gangwon (aHR, 1.38; 95% CI, 1.09~1.74; p<0.01), Jeolla/Gwangju (aHR, 1.41; 95% CI, 1.19~1.67; p<0.01), and Gyeongsang/Busan/Daegu/Ulsan (aHR, 1.37; 95% CI, 1.19~1.59; p<0.01) had a significantly high risk of cerebral infarction.</p><p><strong>Conclusion: </strong>We found there were regional differences in cardiovascular risk and associated risk factors in gout patients. Physicians should screen gout patients for cardiovascular risk profiles in order to facilitate prompt diagnosis and treatment.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0c/bd/jrd-30-3-185.PMC10351371.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10208819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
www.jrd.or.kr Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for controlling pain and inflammation in rheumatic and musculoskeletal diseases. NSAIDs reduce the production of prostaglandin (PG) by inhibiting cyclooxygenase, thereby reducing inflammation. However, PGs are involved in renal hemodynamics to preserve renal blood flow. PGE2 and PGI2 exert vasodilatory action at the afferent arteriole, which maintains glomerular filtration and blood supply to the kidney [1]. Therefore, inhibition of PGs by NSAIDs can cause vasoconstriction of afferent arterioles and leads to renal injury. In addition, PGs also play roles in the regulation of systemic blood volume and blood pressure. By inhibiting natriuresis and diuresis, NSAIDs can cause sodium and water retention and blood pressure elevation [1]. Previous cohort studies have shown that NSAID use can have negative impacts on renal function. Dose-response relationships between NSAID cumulative dose and changes in renal function have been observed in community-based elderly populations [2]. In a retrospective longitudinal cohort study of US Army soldiers, the highest exposure level of NSAIDs was associated with modest but significant increases of acute kidney injury and chronic kidney disease [3]. These findings highlight concerns regarding renal toxicity associated with long-term use of NSAIDs in patients with ankylosing spondylitis (AS). A recent study by Koo et al. [4] published in the Journal of Rheumatic Diseases investigated the relationship between longterm use of NSAIDs and renal function using the electronic medical records of 1,280 patients with AS. NSAID exposure was determined by the Assessment of Spondyloarthritis International Society (ASAS) NSAID Intake Score for time intervals of 6 months, 1 year, 2 years, 3 years, 5 years, and 10 years. The authors concluded that there was no clinically significant correlation between NSAID Intake Score and change in estimated glomerular filtration rate (eGFR) in AS patients. To interpret the results of this study, some points need to be considered. First, the finding that there was no clinically significant deterioration of renal function in patients treated with higher doses of NSAIDs might be due to channeling bias, where patients with better renal function and less comorbidities may have been prescribed more NSAIDs than those with poorer renal function and more comorbidities. In a Swedish national population-based cohort study of spondyloarthritis patients examining the cardiovascular and renal safety of nonselective NSAIDs and selective COX-2 inhibitors, the relative risk of renal insufficiency was higher in the NSAID-nonexposed group compared with the nonselective NSAID-exposed group, reflecting selection of patients being prescribed NSAIDs [5]. Second, considering the young age of the study population, relatively few patients experienced decline in renal function. In the ASAScomorbidities in spondyloarthritis (COMOSPA) cohort, the
{"title":"Are nonsteroidal anti-inflammatory drugs safe for the kidney in ankylosing spondylitis?","authors":"Ji-Won Kim","doi":"10.4078/jrd.2023.0033","DOIUrl":"https://doi.org/10.4078/jrd.2023.0033","url":null,"abstract":"www.jrd.or.kr Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for controlling pain and inflammation in rheumatic and musculoskeletal diseases. NSAIDs reduce the production of prostaglandin (PG) by inhibiting cyclooxygenase, thereby reducing inflammation. However, PGs are involved in renal hemodynamics to preserve renal blood flow. PGE2 and PGI2 exert vasodilatory action at the afferent arteriole, which maintains glomerular filtration and blood supply to the kidney [1]. Therefore, inhibition of PGs by NSAIDs can cause vasoconstriction of afferent arterioles and leads to renal injury. In addition, PGs also play roles in the regulation of systemic blood volume and blood pressure. By inhibiting natriuresis and diuresis, NSAIDs can cause sodium and water retention and blood pressure elevation [1]. Previous cohort studies have shown that NSAID use can have negative impacts on renal function. Dose-response relationships between NSAID cumulative dose and changes in renal function have been observed in community-based elderly populations [2]. In a retrospective longitudinal cohort study of US Army soldiers, the highest exposure level of NSAIDs was associated with modest but significant increases of acute kidney injury and chronic kidney disease [3]. These findings highlight concerns regarding renal toxicity associated with long-term use of NSAIDs in patients with ankylosing spondylitis (AS). A recent study by Koo et al. [4] published in the Journal of Rheumatic Diseases investigated the relationship between longterm use of NSAIDs and renal function using the electronic medical records of 1,280 patients with AS. NSAID exposure was determined by the Assessment of Spondyloarthritis International Society (ASAS) NSAID Intake Score for time intervals of 6 months, 1 year, 2 years, 3 years, 5 years, and 10 years. The authors concluded that there was no clinically significant correlation between NSAID Intake Score and change in estimated glomerular filtration rate (eGFR) in AS patients. To interpret the results of this study, some points need to be considered. First, the finding that there was no clinically significant deterioration of renal function in patients treated with higher doses of NSAIDs might be due to channeling bias, where patients with better renal function and less comorbidities may have been prescribed more NSAIDs than those with poorer renal function and more comorbidities. In a Swedish national population-based cohort study of spondyloarthritis patients examining the cardiovascular and renal safety of nonselective NSAIDs and selective COX-2 inhibitors, the relative risk of renal insufficiency was higher in the NSAID-nonexposed group compared with the nonselective NSAID-exposed group, reflecting selection of patients being prescribed NSAIDs [5]. Second, considering the young age of the study population, relatively few patients experienced decline in renal function. In the ASAScomorbidities in spondyloarthritis (COMOSPA) cohort, the","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/43/8b/jrd-30-3-139.PMC10351374.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9928881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mi Ryoung Seo, Jina Yeo, Jun Won Park, Yeon-Ah Lee, Ju Ho Lee, Eun Ha Kang, Seon Mi Ji, Seong-Ryul Kwon, Seong-Kyu Kim, Tae-Jong Kim, Tae-Hwan Kim, Hye Won Kim, Min-Chan Park, Kichul Shin, Sang-Hoon Lee, Eun Young Lee, Hoon Suk Cha, Seung Cheol Shim, Youngim Yoon, Seung Ho Lee, Jun Hong Lim, Han Joo Baek
We aimed to develop evidence-based recommendations for treating axial spondylarthritis (axSpA) in Korea. The development committee was constructed, key clinical questions were determined, and the evidence was searched through online databases including MEDLINE, Embase, Cochrane, KoreaMed, and KMbase. Systematic literature reviews were conducted, quality of evidence was determined, and draft recommendations were formulated according to the Grading of Recommendations Assessment, Development, and Evaluations methodology. Recommendations that reached 80% consensus among a voting panel were finalized. Three principles and 21 recommendations were determined. Recommendations 1 and 2 pertain to treatment strategies, regular disease status assessment, and rheumatologist-steered multidisciplinary management. Recommendations 3 and 4 strongly recommend patient education, exercise, and smoking cessation. Recommendations 5~12 address pharmacological treatment of active disease using nonsteroidal anti-inflammatory drugs, glucocorticoids, sulfasalazine, biologics, and Janus kinase inhibitors. Recommendations 13~16 address treatment in stable disease. We suggest against spa and acupuncture as therapies (Recommendation 17). Recommendations 18 and 19 pertain to total hip arthroplasty and spinal surgery. Monitoring of comorbidities and drug toxicities are recommended (Recommendations 20 and 21). Recommendations for axSpA treatment in a Korean context were developed based on comprehensive clinical questions and evidence. These are intended to guide best practice in the treatment of axSpA.
{"title":"Korean treatment recommendations for patients with axial spondyloarthritis.","authors":"Mi Ryoung Seo, Jina Yeo, Jun Won Park, Yeon-Ah Lee, Ju Ho Lee, Eun Ha Kang, Seon Mi Ji, Seong-Ryul Kwon, Seong-Kyu Kim, Tae-Jong Kim, Tae-Hwan Kim, Hye Won Kim, Min-Chan Park, Kichul Shin, Sang-Hoon Lee, Eun Young Lee, Hoon Suk Cha, Seung Cheol Shim, Youngim Yoon, Seung Ho Lee, Jun Hong Lim, Han Joo Baek","doi":"10.4078/jrd.2023.0025","DOIUrl":"10.4078/jrd.2023.0025","url":null,"abstract":"<p><p>We aimed to develop evidence-based recommendations for treating axial spondylarthritis (axSpA) in Korea. The development committee was constructed, key clinical questions were determined, and the evidence was searched through online databases including MEDLINE, Embase, Cochrane, KoreaMed, and KMbase. Systematic literature reviews were conducted, quality of evidence was determined, and draft recommendations were formulated according to the Grading of Recommendations Assessment, Development, and Evaluations methodology. Recommendations that reached 80% consensus among a voting panel were finalized. Three principles and 21 recommendations were determined. Recommendations 1 and 2 pertain to treatment strategies, regular disease status assessment, and rheumatologist-steered multidisciplinary management. Recommendations 3 and 4 strongly recommend patient education, exercise, and smoking cessation. Recommendations 5~12 address pharmacological treatment of active disease using nonsteroidal anti-inflammatory drugs, glucocorticoids, sulfasalazine, biologics, and Janus kinase inhibitors. Recommendations 13~16 address treatment in stable disease. We suggest against spa and acupuncture as therapies (Recommendation 17). Recommendations 18 and 19 pertain to total hip arthroplasty and spinal surgery. Monitoring of comorbidities and drug toxicities are recommended (Recommendations 20 and 21). Recommendations for axSpA treatment in a Korean context were developed based on comprehensive clinical questions and evidence. These are intended to guide best practice in the treatment of axSpA.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9f/95/jrd-30-3-151.PMC10351367.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9851657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: Systemic lupus erythematosus (SLE) is an autoimmune disease, characterized by the production of autoantibodies and high cholesterol levels. HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors have exhibited anti-inflammatory effects in several clinical trials. We conducted this study to evaluate the effect of rosuvastatin on inflammatory responses in lupus-prone mice.
Methods: MRL/lpr mice were intraperitoneally injected with rosuvastatin (10 mg/kg, n=4) or vehicle (2% dimethyl sulfoxide, n=4) five times a week from 13 to 17 weeks of age. The serum levels of low-density lipoprotein (LDL) cholesterol and autoantibodies were measured, as well as the urine levels of albumin. Renal tissues were stained for histopathological analysis. Concentrations of key inflammatory cytokines were measured in the serum, and messenger RNA (mRNA) levels in target organs (kidney, spleen, and lymph nodes) were evaluated.
Results: Rosuvastatin treatment significantly decreased serum LDL cholesterol concentration in MRL/lpr mice. However, the clinical manifestations and autoantibody titres did not improve with rosuvastatin treatment. In addition, serum inflammatory cytokines and proteinuria did not change. Histopathological analysis of the kidneys revealed no improvement. When assessing the expression of mRNA, treatment with rosuvastatin decreased tumor necrosis alpha and interleukin-17 concentration in spleen and kidney tissue and in the kidneys and lymph nodes of MRL/lpr mice, respectively.
Conclusion: Although it can decrease inflammatory cytokines in the lymphoid organs and kidneys of MRL/lpr mice, treatment with rosuvastatin is insufficient to alleviate SLE.
{"title":"Rosuvastatin treatment alone cannot alleviate lupus in murine model: a pilot study.","authors":"Wook-Young Baek, Sung-Min Lee, Sang-Won Lee, Chang-Hee Suh","doi":"10.4078/jrd.2023.0021","DOIUrl":"https://doi.org/10.4078/jrd.2023.0021","url":null,"abstract":"<p><strong>Objective: </strong>Systemic lupus erythematosus (SLE) is an autoimmune disease, characterized by the production of autoantibodies and high cholesterol levels. HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors have exhibited anti-inflammatory effects in several clinical trials. We conducted this study to evaluate the effect of rosuvastatin on inflammatory responses in lupus-prone mice.</p><p><strong>Methods: </strong>MRL/<i>lpr</i> mice were intraperitoneally injected with rosuvastatin (10 mg/kg, n=4) or vehicle (2% dimethyl sulfoxide, n=4) five times a week from 13 to 17 weeks of age. The serum levels of low-density lipoprotein (LDL) cholesterol and autoantibodies were measured, as well as the urine levels of albumin. Renal tissues were stained for histopathological analysis. Concentrations of key inflammatory cytokines were measured in the serum, and messenger RNA (mRNA) levels in target organs (kidney, spleen, and lymph nodes) were evaluated.</p><p><strong>Results: </strong>Rosuvastatin treatment significantly decreased serum LDL cholesterol concentration in MRL/<i>lpr</i> mice. However, the clinical manifestations and autoantibody titres did not improve with rosuvastatin treatment. In addition, serum inflammatory cytokines and proteinuria did not change. Histopathological analysis of the kidneys revealed no improvement. When assessing the expression of mRNA, treatment with rosuvastatin decreased tumor necrosis alpha and interleukin-17 concentration in spleen and kidney tissue and in the kidneys and lymph nodes of MRL/<i>lpr</i> mice, respectively.</p><p><strong>Conclusion: </strong>Although it can decrease inflammatory cytokines in the lymphoid organs and kidneys of MRL/<i>lpr</i> mice, treatment with rosuvastatin is insufficient to alleviate SLE.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/17/cb/jrd-30-3-198.PMC10351369.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9904865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hand involvement in sarcoidosis is rare and it presents as tenosynovitis, dactylitis, nodules and osteoarticular bony destruction. We describe an unusual presentation of progressive intrinsic muscle contracture of both hands in a 42-year-old woman with sarcoid myopathy who presented with painful swelling and weakness of all four extremities. Her systemic symptoms improved with oral corticosteroids, but the hand muscle contracture remained after resolution of myositis. Serial soft tissue releases of intrinsic muscle contracture improved hand function markedly. This case highlights that surgery is a viable option to treat intrinsic muscle contracture in patients with chronic sarcoid myopathy complicated with severe muscle contracture.
{"title":"Intrinsic contracture of the hands in sarcoid myopathy.","authors":"Siew Khei Liew, Jin Kyun Park, Hyun Sik Gong","doi":"10.4078/jrd.2023.0007","DOIUrl":"https://doi.org/10.4078/jrd.2023.0007","url":null,"abstract":"<p><p>Hand involvement in sarcoidosis is rare and it presents as tenosynovitis, dactylitis, nodules and osteoarticular bony destruction. We describe an unusual presentation of progressive intrinsic muscle contracture of both hands in a 42-year-old woman with sarcoid myopathy who presented with painful swelling and weakness of all four extremities. Her systemic symptoms improved with oral corticosteroids, but the hand muscle contracture remained after resolution of myositis. Serial soft tissue releases of intrinsic muscle contracture improved hand function markedly. This case highlights that surgery is a viable option to treat intrinsic muscle contracture in patients with chronic sarcoid myopathy complicated with severe muscle contracture.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2d/ca/jrd-30-3-204.PMC10351373.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10208818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-01Epub Date: 2023-05-04DOI: 10.4078/jrd.2023.0004
Ah-Ra Choi, Ji-Hyoun Kang, Ki-Jeong Park, Hae-In Lee, Tae-Jong Kim
Objective: The objective of this study was to evaluate the safety and efficacy of light-emitting diode therapy (LEDT) in the management of pain and stiffness in patients with refractory hand tenosynovitis to non-steroidal anti-inflammatory drugs.
Methods: A total of 12 patients were enrolled in the study and received LEDT twice a week for four weeks. Sociodemographic, clinical, and laboratory data were collected, and the visual analog scale (VAS) pain and stiffness scores of each hand were assessed every two weeks. The thickness of the flexor tendon in the patients' hand was evaluated using ultrasonography. To investigate the molecular effects of LEDT, we measured the expression levels of type III collagen in tendon cells, with and without LEDT treatment.
Results: After undergoing LEDT, participants showed clinically significant improvements in VAS pain scores at weeks 2, 4, and 8 compared to their baseline, and in VAS stiffness scores at weeks 4 and 8. According to the ultrasonography results, there was a decreasing tendency in tendon thickness for each finger in week 8 compared to the baseline, but the difference was not statistically significant. No adverse events were reported. Additionally, our results indicated a significant increase in type III collagen levels in the LEDT group compared to the control group (1.48±0.18 vs. 0.99±0.02, p=0.031), indicating a potential molecular mechanism for the observed clinical improvements.
Conclusion: LEDT may provide a viable alternative to pharmacological treatments in the future, due to its simple and easy method of administration.
{"title":"Effects of light-emitting diode therapy on hand stiffness and pain in non-steroidal anti-inflammatory drug-refractory patients with tenosynovitis.","authors":"Ah-Ra Choi, Ji-Hyoun Kang, Ki-Jeong Park, Hae-In Lee, Tae-Jong Kim","doi":"10.4078/jrd.2023.0004","DOIUrl":"10.4078/jrd.2023.0004","url":null,"abstract":"<p><strong>Objective: </strong>The objective of this study was to evaluate the safety and efficacy of light-emitting diode therapy (LEDT) in the management of pain and stiffness in patients with refractory hand tenosynovitis to non-steroidal anti-inflammatory drugs.</p><p><strong>Methods: </strong>A total of 12 patients were enrolled in the study and received LEDT twice a week for four weeks. Sociodemographic, clinical, and laboratory data were collected, and the visual analog scale (VAS) pain and stiffness scores of each hand were assessed every two weeks. The thickness of the flexor tendon in the patients' hand was evaluated using ultrasonography. To investigate the molecular effects of LEDT, we measured the expression levels of type III collagen in tendon cells, with and without LEDT treatment.</p><p><strong>Results: </strong>After undergoing LEDT, participants showed clinically significant improvements in VAS pain scores at weeks 2, 4, and 8 compared to their baseline, and in VAS stiffness scores at weeks 4 and 8. According to the ultrasonography results, there was a decreasing tendency in tendon thickness for each finger in week 8 compared to the baseline, but the difference was not statistically significant. No adverse events were reported. Additionally, our results indicated a significant increase in type III collagen levels in the LEDT group compared to the control group (1.48±0.18 vs. 0.99±0.02, p=0.031), indicating a potential molecular mechanism for the observed clinical improvements.</p><p><strong>Conclusion: </strong>LEDT may provide a viable alternative to pharmacological treatments in the future, due to its simple and easy method of administration.</p>","PeriodicalId":56161,"journal":{"name":"Journal of Rheumatic Diseases","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c8/95/jrd-30-3-170.PMC10351370.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9904862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}